癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
KSR1 Antibody (N-term A7)
Purified Rabbit Polyclonal Antibody (Pab)
- 产品详情
- 实验流程
- 背景知识
Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | Q8IVT5 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 102160 Da |
| Antigen Region | 1-30 aa |
| Gene ID | 8844 |
|---|---|
| Other Names | Kinase suppressor of Ras 1, KSR1, KSR |
| Target/Specificity | This KSR1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human KSR1. |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 E~~Use at an assay dependent concentration. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | KSR1 Antibody (N-term A7) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | KSR1 |
|---|---|
| Synonyms | KSR |
| Function | Part of a multiprotein signaling complex which promotes phosphorylation of Raf family members and activation of downstream MAP kinases (By similarity). Independently of its kinase activity, acts as MAP2K1/MEK1 and MAP2K2/MEK2-dependent allosteric activator of BRAF; upon binding to MAP2K1/MEK1 or MAP2K2/MEK2, dimerizes with BRAF and promotes BRAF-mediated phosphorylation of MAP2K1/MEK1 and/or MAP2K2/MEK2 (PubMed:29433126). Promotes activation of MAPK1 and/or MAPK3, both in response to EGF and to cAMP (By similarity). Its kinase activity is unsure (By similarity). Some protein kinase activity has been detected in vitro, however the physiological relevance of this activity is unknown (By similarity). |
| Cellular Location | Cytoplasm. Membrane; Peripheral membrane protein. Cell membrane {ECO:0000250|UniProtKB:Q61097}; Peripheral membrane protein {ECO:0000250|UniProtKB:Q61097}. Cell projection, ruffle membrane {ECO:0000250|UniProtKB:Q61097}. Endoplasmic reticulum membrane. Note=In unstimulated cells, where the phosphorylated form is bound to a 14-3-3 protein, sequestration in the cytoplasm occurs. Following growth factor treatment, the protein is free for membrane translocation, and it moves from the cytoplasm to the cell periphery. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Protein kinases are enzymes that transfer a phosphate group from a phosphate donor, generally the g phosphate of ATP, onto an acceptor amino acid in a substrate protein. By this basic mechanism, protein kinases mediate most of the signal transduction in eukaryotic cells, regulating cellular metabolism, transcription, cell cycle progression, cytoskeletal rearrangement and cell movement, apoptosis, and differentiation. With more than 500 gene products, the protein kinase family is one of the largest families of proteins in eukaryotes. The family has been classified in 8 major groups based on sequence comparison of their tyrosine (PTK) or serine/threonine (STK) kinase catalytic domains. The STE group (homologs of yeast Sterile 7, 11, 20 kinases) consists of 50 kinases related to the mitogen-activated protein kinase (MAPK) cascade families (Ste7/MAP2K, Ste11/MAP3K, and Ste20/MAP4K). MAP kinase cascades, consisting of a MAPK and one or more upstream regulatory kinases (MAPKKs) have been best characterized in the yeast pheromone response pathway. Pheromones bind to Ste cell surface receptors and activate yeast MAPK pathway.
REFERENCES
Blume-Jensen P, et al. Nature 2001. 411: 355.
Cantrell D, J. Cell Sci. 2001. 114: 1439.
Jhiang S Oncogene 2000. 19: 5590.
Manning G, et al. Science 2002. 298: 1912.
Moller, D, et al. Am. J. Physiol. 1994. 266: C351-C359.
Robertson, S. et al. Trends Genet. 2000. 16: 368.
Robinson D, et al. Oncogene 2000. 19: 5548.
Van der Ven, P, et al. Hum. Molec. Genet. 1993. 2: 1889.
Vanhaesebroeck, B, et al. Biochem. J. 2000. 346: 561.
Van Weering D, et al. Recent Results Cancer Res. 1998. 154: 271.
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